沙眼衣原体感染活化NOD1信号通路的研究  

A Study on the Activation of NOD1 Signaling Pathway Induced by Chlamydia trachomatis Infection

作　　者：芦玲[1] 肖丽佳[1] 曾建兴[1] 朱权[1] 王芙艳[1] 余平[1] 

机构地区：[1]中南大学基础医学院免疫学系,湖南长沙410078

出　　处：《激光生物学报》2017年第1期61-67,共7页Acta Laser Biology Sinica

基　　金：国家自然科学基金项目(81572040)

摘　　要：目的:探索沙眼衣原体(Chlamydia trachomatis,Ct)持续感染状态下,NOD1、IL-6及STAT3分子的表达情况和相互关系。方法:利用HeLa229细胞或STAT3基因沉默的HeLa229细胞,分别建立沙眼衣原体的急性感染和持续感染模型;应用Western Blot及ELISA等方法检测不同感染状态下STAT3及NOD1蛋白表达水平以及细胞因子IL-6的分泌水平。结果:HeLa229细胞在Ct感染状态下,STAT3和NOD1以及IL-6表达水平均升高,且于持续感染状态下的升高较急性感染状态下的升高更明显;沉默STAT3基因后,Ct感染的细胞NOD1及IL-6的表达水平下降明显。结论:HeLa229细胞在Ct持续感染状态下,STAT3能上调NOD1及IL-6表达水平,上述分子间存在NOD1-IL-6-STAT3正反馈信号通路。Objective ： To study the expression level of NODI , IL-6 and STAT3 in the model of Chlamydia trachomatis （Ct） persistent infection, and explore the connection and effects between those molecules. Methods： We established the acute infection model and the persistent infection model by using the HeLa229 or stable STAT3 knockdown HeLa229 cell line. Western Bolt and ELISA were performed respectively to detect the expression levels of STAT3 and NODI and the secretion of inflammatory cytokines IL-6 in the different infection states. Results： We found that the expression lev-els of STAT3, NODI and IL-6 were up regulated in the acute and persistent infection models, and there was even higher expression level in the persistent infection model. Our study suggested that the levels of IL-6 and NODI declined signifi-cantly in the persistent infection model when the gene of STAT3 was silenced. Conclusions ： The signal transduction pathway of STAT3-NODI-IL-6 was activated in the persistent Ct infection model. STAT3 up-regulated the expression of NODI and promoted the secretion of IL-6 to intensify the intracellular inflammation.

关 键 词：沙眼衣原体 持续感染 NOD1 IL-6 STAT3 

分 类 号：R392.1[医药卫生—免疫学]